631 research outputs found

    A new proof for the decidability of D0L ultimate periodicity

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    We give a new proof for the decidability of the D0L ultimate periodicity problem based on the decidability of p-periodicity of morphic words adapted to the approach of Harju and Linna.Comment: In Proceedings WORDS 2011, arXiv:1108.341

    A global reanalysis of nuclear parton distribution functions

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    We determine the nuclear modifications of parton distribution functions of bound protons at scales Q2≥1.69Q^2\ge 1.69 GeV2^2 and momentum fractions 10−5≤x≤110^{-5}\le x\le 1 in a global analysis which utilizes nuclear hard process data, sum rules and leading-order DGLAP scale evolution. The main improvements over our earlier work {\em EKS98} are the automated χ2\chi^2 minimization, simplified and better controllable fit functions, and most importantly, the possibility for error estimates. The resulting 16-parameter fit to the N=514 datapoints is good, χ2/d.o.f=0.82\chi^2/{\rm d.o.f}=0.82. Within the error estimates obtained, the old {\em EKS98} parametrization is found to be fully consistent with the present analysis, with no essential difference in terms of χ2\chi^2 either. We also determine separate uncertainty bands for the nuclear gluon and sea quark modifications in the large-xx region where they are not stringently constrained by the available data. Comparison with other global analyses is shown and uncertainties demonstrated. Finally, we show that RHIC-BRAHMS data for inclusive hadron production in d+Au collisions lend support for a stronger gluon shadowing at x<0.01x<0.01 and also that fairly large changes in the gluon modifications do not rapidly deteriorate the goodness of the overall fits, as long as the initial gluon modifications in the region x∼0.02−0.04x\sim 0.02-0.04 remain small.Comment: 33 pages, 14 figure

    Radiative lifetime measurements of rubidium Rydberg states

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    We have measured the radiative lifetimes of ns, np and nd Rydberg states of rubidium in the range 28 < n < 45. To enable long-lived states to be measured, our experiment uses slow-moving Rb atoms in a magneto-optical trap (MOT). Two experimental techniques have been adopted to reduce random and systematic errors. First, a narrow-bandwidth pulsed laser is used to excite the target Rydberg state, resulting in minimal shot-to-shot variation in the initial state population. Second, we monitor the target state population as a function of time delay from the laser pulse using a short-duration, millimetre-wave pulse that is resonant with a one- or two-photon transition. We then selectively field ionize the monitor state, and detect the resulting electrons with a micro-channel plate. This signal is an accurate mirror of the target state population, and is uncontaminated by contributions from other states which are populated by black body radiation. Our results are generally consistent with other recent experimental results obtained using a less sensitive method, and are also in excellent agreement with theory.Comment: 27 pages,6 figure

    Valosin-Containing Protein (VCP) Disease and Familial Alzheimer’s Disease: Contrasts and Overlaps

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    Introduction Contrasts between two entities may be illuminating because of the emphasis on what each is not. Here we describe two proteinopathies producing brain neurodegeneration in mature adults, autosomal dominant valosin-containing protein (VCP) disease and Familial Alzheimer’s disease (FAD) caused by presenillin-1 (PSEN1) mutations, illustrating both contrasting patterns of clinical presentation and known neuropathologic and imaging features, and points of congruence

    TiF1-Gamma Plays an Essential Role in Murine Hematopoiesis and Regulates Transcriptional Elongation of Erythroid Genes

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    Transcriptional regulators play critical roles in the regulation of cell fate during hematopoiesis. Previous studies in zebrafish have identified an essential role for the transcriptional intermediary factor TIF1γ in erythropoiesis by regulating the transcription elongation of erythroid genes. To study if TIF1γ plays a similar role in murine erythropoiesis and to assess its function in other blood lineages, we generated mouse models with hematopoietic deletion of TIF1γ. Our results showed a block in erythroid maturation in the bone marrow following tif1γ deletion that was compensated with enhanced spleen erythropoiesis. Further analyses revealed a defect in transcription elongation of erythroid genes in the bone marrow. In addition, loss of TIF1γ resulted in defects in other blood compartments, including a profound loss of B cells, a dramatic expansion of granulocytes and decreased HSC function. TIF1γ exerts its functions in a cell-autonomous manner as revealed by competitive transplantation experiments. Our study therefore demonstrates that TIF1γ plays essential roles in multiple murine blood lineages and that its function in transcription elongation is evolutionally conserved.Stem Cell and Regenerative Biolog

    Revisiting left atrial volumetry by magnetic resonance imaging : the role of atrial shape and 3D angle between left ventricular and left atrial axis

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    Background Accurate measurement of left atrial (LA) volumes is needed in cardiac diagnostics and the follow up of heart and valvular diseases. Geometrical assumptions with 2D methods for LA volume estimation contribute to volume misestimation. In this study, we test agreement of 3D and 2D methods of LA volume detection and explore contribution of 3D LA axis orientation and LA shape in introducing error in 2D methods by cardiovascular magnetic resonance imaging. Methods 30 patients with prior first-ever ischemic stroke and no known heart disease, and 30 healthy controls were enrolled (age 18-49) in a substudy of a prospective case-control study. All study subjects underwent cardiac magnetic resonance imaging and were pooled for this methodological study. LA volumes were calculated by biplane area-length method from both conventional long axis (LAV(AL-LV)) and LA long axis-oriented images (LAV(AL-LA)) and were compared to 3D segmented LA volume (LAV(SAX)) to assess accuracy of volume detection. 3D orientation of LA long axis to left ventricular (LV) long axis and to four-chamber plane were determined, and LA 3D sphericity indices were calculated to assess sources of error in LA volume calculation. Shapiro-Wilk test, Bland-Altman analysis, intraclass and Pearson correlation, and Spearman's rho were used for statistical analysis. Results Biases were - 9.9 mL (- 12.5 to - 7.2) for LAV(AL-LV) and 13.4 (10.0-16.9) for LAV(AL-LA) [mean difference to LAV(SAX) (95% confidence interval)]. End-diastolic LA long axis 3D deviation angle to LV long axis was 28.3 +/- 6.2 degrees [mean +/- SD] and LA long axis 3D rotation angle to four-chamber plane 20.5 +/- 18.0 degrees. 3D orientation of LA axis or 3D sphericity were not correlated to error in LA volume calculation. Conclusions Calculated LA volume accuracy did not improve by using LA long axis-oriented images for volume calculation in comparison to conventional method. We present novel data on LA axis orientation and a novel metric of LA sphericity and conclude that these measures cannot be utilized to assess error in LA volume calculation.Peer reviewe

    Syndecan-4 tunes cell mechanics by activating the kindlin-integrin-RhoA pathway

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    A mechanism of cell response to localized tension shows that syndecan-4 synergizes with EGFR to elicit a mechanosignalling cascade that leads to adaptive cell stiffening through PI3K/kindlin-2 mediated integrin activation. Extensive research over the past decades has identified integrins to be the primary transmembrane receptors that enable cells to respond to external mechanical cues. We reveal here a mechanism whereby syndecan-4 tunes cell mechanics in response to localized tension via a coordinated mechanochemical signalling response that involves activation of two other receptors: epidermal growth factor receptor and beta 1 integrin. Tension on syndecan-4 induces cell-wide activation of the kindlin-2/beta 1 integrin/RhoA axis in a PI3K-dependent manner. Furthermore, syndecan-4-mediated tension at the cell-extracellular matrix interface is required for yes-associated protein activation. Extracellular tension on syndecan-4 triggers a conformational change in the cytoplasmic domain, the variable region of which is indispensable for the mechanical adaptation to force, facilitating the assembly of a syndecan-4/alpha-actinin/F-actin molecular scaffold at the bead adhesion. This mechanotransduction pathway for syndecan-4 should have immediate implications for the broader field of mechanobiology.Peer reviewe

    Progression of herpesvirus infection remodels mitochondrial organization and metabolism

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    Viruses target mitochondria to promote their replication, and infection-induced stress during the progression of infection leads to the regulation of antiviral defenses and mitochondrial metabolism which are opposed by counteracting viral factors. The precise structural and functional changes that underlie how mitochondria react to the infection remain largely unclear. Here we show extensive transcriptional remodeling of protein-encoding host genes involved in the respiratory chain, apoptosis, and structural organization of mitochondria as herpes simplex virus type 1 lytic infection proceeds from early to late stages of infection. High-resolution microscopy and interaction analyses unveiled infection-induced emergence of rough, thin, and elongated mitochondria relocalized to the perinuclear area, a significant increase in the number and clustering of endoplasmic reticulum-mitochondria contact sites, and thickening and shortening of mitochondrial cristae. Finally, metabolic analyses demonstrated that reactivation of ATP production is accompanied by increased mitochondrial Ca2+ content and proton leakage as the infection proceeds. Overall, the significant structural and functional changes in the mitochondria triggered by the viral invasion are tightly connected to the progression of the virus infection
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